2

The Biomedical
Model
what’s
ahead
? In this chapter we consider a model that explains mental disorders
in the same terms as physical illnesses are explained; as being
caused by the disruption or malfunction of biological processes. We
consider the evidence for the role of genes and the biochemistry of
the nervous system in mental disorder. Having looked at the role of
biology in explaining the origin of mental disorder, we will then
focus on some of the treatments such an approach offers. The
rather controversial therapies of drugs, ECT and psychosurgery will
be considered, together with the considerable changes that have
occurred in the application of such treatments since they were first
introduced. Finally, we will discuss a promising new alternative to
ECT, Transcranial Magnetic Brain Stimulation.

Assumptions of the approach

The biomedical model (or disease model) of psychopathology views
psychological disorders as being caused by biological malfunction or
disruption. Biomedical approaches to treatment are based on the idea
that we can correct, or at least reduce, the effects of these malfunctions
or disruption.

• Mental disorder can be understood as illness in the same way as

physical conditions. It can thus be classified, diagnosed and treated by
medical personnel in the same way as physical disease.

• The emphasis of the explanations is on the physiological aspects of

mental disorder rather than its behavioural, thinking or emotional
aspects. For example, the physiological approach would explain

25
Angles on Atypical Psychology

depression in terms of an imbalance of biochemical substances in the

brain, such as serotonin, rather than in terms of low self-esteem,
feelings of helplessness, irrational thinking and so on. This emphasis
on physiology is, of course, on a theoretical level and does not suggest
that medical practitioners are not also concerned with cognitive and
emotional aspects of mental disorder.

• The symptoms of mental disorder can be understood in terms of

malfunction of or disruption to biological systems. For example, this
may involve the abnormal development of part of the nervous system
or neurotransmitters that are too high or too low. The underlying
causes of these symptoms are also biological in origin, for example
faulty genes or brain damage.

• Mental disorder can be treated by physiologically based approaches,

including drugs, surgery and the application of electric shocks,
magnetic fields and bright light.
The biomedical position is one with a very long history – indeed, the very
language of psychopathology is grounded in the medical model, the most
obvious example being that such conditions are often called mental
illnesses. At one time all mental disorders were seen by some as being
caused entirely by biological factors but most people now consider this
position as untenable and recognise that most, if not all, psychological
conditions (and some physical illnesses) are the result of a complex inter-
action of physiology and environment. There is considerable variability in
the extent to which specific conditions can be explained in terms of
biology, which is hardly surprising given the enormous range of clinical
conditions that exist. In order to investigate the role of physical factors in
the origins of mental illness, psychologists have pursued several avenues
of research including the ones we will consider here, the role of genes and
the biochemistry of the nervous system.

The role of genes

Behaviour genetics is the study of individual differences in psychological
characteristics that are attributable in part to differences in genetic
makeup. Before we consider the effects that genes may have on abnormal
behaviour, it is useful to briefly discuss how genes are inherited and the
way in which they exert an effect.
Human beings have 46 chromosomes (23 pairs) in every cell of their
bodies except in the ova (eggs) and sperm, in which there are 23, one of
each pair. Via the egg and sperm, a child randomly inherits half its
chromosomes from the mother and half from the father. Each
chromosome is made up of thousands of genes, which are the carriers of
the genetic information (DNA) that is passed from parent to child.

26
 Chapter 2 The Biomedical Model

The total genetic makeup of an individual is known as the genotype.

Genes contain the instructions for producing a physical body, which in
turn have an effect on psychological characteristics. The observable
physical and behavioural characteristics of an individual are known
collectively as their phenotype. The phenotype is the result of both genetic
and environmental influences. For example, two children may be born
with a similarly high predisposition to suffer anxiety. If one then experi-
ences a very stressful environment, he may become a very anxious adult
and perhaps be prone to anxiety disorders such as phobias. The other
may, in contrast, have a supportive and benign upbringing that results in
a well-adjusted adult capable of coping well with anxiety provoking situa-
tions. Their genotypes are similar, but their phenotypes are very different.
It is also possible that the genotype can produce experiences that may result
in a certain phenotype. By their influence on brain chemistry genes may, for
example, have the direct influence of producing timidity in a baby boy. This
may then have certain indirect consequences, for example, it may cause his
mother to protect him and his peers to mock him. This in turn increases his
timidity. The genotype has therefore had an indirect effect on the phenotype.
What is important to note is that psychopathological conditions are
disorders of the phenotype, not the genotype. People do not, for example,
inherit genes for such conditions as schizophrenia or an anxiety disorder.
Rather, they inherit genes that make them vulnerable to the disorder.
They inherit a genotype for the vulnerability, also known as the diathesis,
but not the condition itself. This is expressed in the diathesis-stress model,
which states that a combination of both genetic vulnerability and environ-
mental stress produces mental disorders. Whether the genotype will
eventually translate into the phenotype depends on many environmental
factors. The potential effects that genes have on clinical syndromes (such
as mental disorders) have been investigated by conducting family studies,
twin studies and adoption studies. We will consider each in turn.

Family studies
We share 50% of our genes with our parents and our siblings, and 25%
with our aunts, uncles and grandparents. The knowledge of the extent to
which genes within family members are shared provides a means of
testing whether there is a genetic element to certain conditions. If the
correlation between the degree of consanguinity (the amount of shared
genetic material) and the prevalence of a disorder is high, then it is
reasonable to assume that heredity is exerting an influence on the develo-
pment of the particular mental disorder. For example, in Chapter 11 there
is an account of a study by Hetterna et al. (2001), who analysed data on
anxiety disorders from many family studies and found that, overall,
individuals who were closely genetically related to a patient with an
anxiety disorder were 4–6 times more likely than non-related others to
develop an anxiety condition.

27
Angles on Atypical Psychology

Twin studies
One of the most useful ways of studying the contribution of heredity to
any characteristic is to compare the degree of similarity between identical
and non-identical twins. Identical twins, known as monozygotic (MZ)
twins, have identical genetic makeup because they come from the same
fertilised egg or zygote. Non-identical (fraternal) twins are referred to as
dizygotic (DZ) twins because they come from two separate zygotes and
are therefore no more genetically alike than ordinary brothers and sisters.
The degree to which twins are similar on any particular characteristic is
known as the concordance rate. If the concordance rate for MZ twins is
higher than that for DZ twins on a particular characteristic, then this
indicates some heritability of that characteristic. Gottesman (1991)
found a concordance rate for schizophrenia of 17% for DZ twins and a
much higher rate of 48% for MZ twins (referred to in Chapter 8), strongly
suggesting a hereditary element in schizophrenia. McGuffin et al. (1996),
in a study of major depression (severe depression), found a concordance
rate of 46% in MZ twins and 20% in DZ twins (Chapter 9). In contrast,
Kendler et al. (1992) found the concordance rates for mild depression to
be much more similar (49% for MZ and 42% for DZ twins). These two
sets of data indicate a much larger hereditary element in major depression
than in mild depression.
However, we do need to exercise some caution in the interpretation of
data from twin studies. Although higher concordance rates for MZ than
for DZ twins strongly implicate heredity, you can see from the example of
schizophrenia that, whilst MZ twins have identical genetic material, on

Figure 2.1 These twins are

genetically identical but have
nonetheless turned out quite
different in many ways. This
illustrates the importance of the
environment

28
 Chapter 2 The Biomedical Model

average half of the identical twins of people suffering schizophrenia do

not develop the disorder. Therefore other factors (environment and
experience) must also play a part. It is also possible that MZ twins, being
identical, may be treated more similarly than DZ twins, especially if the
DZ twins are not the same sex.
One of the problems of any comparison of concordance rates between
people in the same family is that they share a similar environment, so it is
never clear to what extent their shared experiences rather than heredity
has contributed to a condition (Figure 2.1). One way to try to separate
out the effects of heredity and environment is to look at individuals who
were not raised in their biological families. We will therefore now turn our
attention to adoption studies.

Adoption studies
Comparison of the rates of any mental disorder between adopted children
and both their biological and adoptive parents are another means of
assessing the extent of heredity. The Classic Research section on p. 133
provides an account of an adoption study by Heston (1966), in which it
was demonstrated that 10% of adopted children of mothers with schizo-
phrenia developed the condition themselves. This is exactly the rate that
would be expected in first-degree relatives raised by their biological
mothers and far higher than the rate of 1% in the general population.
Again, this strongly implicates heredity in this condition.

Linkage analysis and molecular genetics

New techniques for studying inheritance of psychological characteristics
come from the field of molecular genetics, which, as the name suggests,
involves studying genes on the molecular level. Molecular geneticists use
linkage analysis to try to ascertain the specific gene involved in a particular
clinical condition. It uses as its starting point genes whose location on a
certain chromosome and whose physical effects are already known, such
as a gene that determines eye colour. Such genes are known as genetic
markers. Blood samples are taken from members of families in which a
particular mental illness is prevalent and used to ascertain the inheri-
tance of the genetic markers. If the occurrence of the mental illness goes
along with a particular genetic marker then it can be assumed that they
are in a similar place on the same chromosome – in other words, that they
are linked. A linkage analysis of the Old Order Amish (Egeland et al.
1987) revealed evidence that bipolar disorder results from a dominant
gene on the eleventh chromosome. These findings have not been repli-
cated but research is ongoing. As yet, the work on linkage analysis is in
the early stages but has progressed quite a long way in some areas such as
Alzheimer’s disease; it will doubtless prove to be of considerable value in
the future.

29
Angles on Atypical Psychology

for and
against
the importance of genes
Evidence from twin, adoption and family studies all points to a role for genes in the
development of mental disorder.

There are sound reasons for questioning the validity of all these methods.

Molecular genetic studies have begun to show us which genes appear to be associated
with mental disorder.

where to
now
?
The following are good sources of further information about behavioural genetics:

Jarvis, M. et al. (2000) Angles on Psychology. Cheltenham: Nelson Thornes – chapter 1

contains a useful account of behavioural genetics research.

The Psychologist, March 2001 – a special edition devoted to papers on behavioural genetics.
Although not exclusively concerned with psychopathology, it is relevant and interesting. The lead
article by Plomin, a great enthusiast for the genetic approach, includes the use of twin studies and
adoption studies with respect to autism. Other papers discuss the issue from various perspectives.
Of particular interest is one by Steven Rose, a biologist who urges caution in applying genetic
explanations to behaviour. All the articles are both thought provoking and readable and will be
useful in various aspects of psychology.

The biochemistry of the nervous

system
The human nervous system is the most important system in the control
of behaviour and the experience of mental events. At the centre of the
nervous system is the brain, which manages all human capacities
including learning, feeling emotions, relating to other people and
perceiving the world. The nervous system is composed of billions of
neurons, highly specialised nerve cells ‘woven into a complex tapestry of
connections and interconnections’ (Dwyer and Scampion, 1996, p. 176).
Neurons are specially adapted to receive, process and/or transmit infor-
mation to other cells. They communicate with each other (and with
muscles and glands) both electrically and chemically. When a neuron is

30
 Chapter 2 The Biomedical Model

stimulated, a wave of electrical voltage called a nerve impulse passes

down the axon to the terminal ending (see Figure 2.2). Between the
nerve ending and the next cell there is a small gap called a synapse, across
which electricity cannot pass. The impulse passes to the next neuron by
means of chemicals called neurotransmitters, chemical messengers that
cross the small distance across the synaptic gap and excite or inhibit the
next neuron. When a neurotransmitter is released, some of it remains in
the synapse and needs to be removed so that the synapse can return to
its normal state. Some is broken down by enzymes while some of it is
pumped back into the neuron from which it came, a process known as
reuptake. If this process is faulty, then problems arise. As we shall see later
in this chapter, and in Chapter 9, some therapeutic drugs operate by
inhibiting the reuptake of certain neurotransmitters.

Figure 2.2 A nerve cell

and synapse

Neurotransmitters play a crucial role in many psychological processes,

including mood and emotion. It is now clear that abnormalities in the
production of neurotransmitters can contribute to psychopathological
conditions. Noradrenaline (also called norepinephrine) has been associated
with anxiety disorders, serotonin may be involved in some types of
depression and eating disorders, and dopamine appears to be implicated
in schizophrenia. Theories linking psychopathology to neurotransmitters
often suggest that too little or too much of a particular neurotransmitter
may be responsible for the condition. It is also possible that the receptors
are at fault – if they are too numerous or too easily excited then this can
have the same effect as too much transmitter being released. One of the
theories of schizophrenia is that the hallucinations and delusions exper-
ienced are the result of an excess of dopamine receptors. The article
below demonstrates how an understanding of brain structure can aid
diagnosis of certain disorders.

31
Angles on Atypical Psychology

research
now
investigating schizophrenia and learning
difficulties using magnetic resonance imaging
(MRI)
Sanderson, T.L., Best, J.J., Doody, G.A., Cunningham Owens, D.G. and Johnstone,
E.C. (1999). Neuroanatomy of comorbid schizophrenia and learning disability: a
controlled study. Lancet, 354, 1867–1870

Aim: To investigate reasons for the relatively high frequency of schizophrenia in learning-
disabled populations and to see whether the major presenting symptom is schizophrenia or
learning disability.

Method: Three groups of patients and one group of normal controls were compared, each
group matched on age and sex:

• 20 patients with learning disability

• 25 patients with schizophrenia
• 23 patients with both disorders
• 29 normal controls.
Each person was given a whole-brain scan; in addition, specific areas of the brain were scanned
(see Figure 2.3).

Figure 2.3 MRI scans have

allowed us to see in much more
detail the structure of the brain.
In some cases this has shown
that mental disorder is linked to
abnormal brain function or
development

Results: The scans of the group with schizophrenia and the group with both learning difficulties
and schizophrenia were very similar in terms of both general structure and the structure of the
amygdala—hippocampus. The amygdala—hippocampus in both groups was significantly smaller

32
 Chapter 2 The Biomedical Model

than those in normal controls. The brains of the learning-disabled patients who did not have schiz-
ophrenia were smaller than those of the other three groups, but the amygdala—hippocampus was
larger. Therefore the brain structure of people with both schizophrenia and learning difficulties
resembles that of people with schizophrenia but not that of those with learning disability.

Conclusions: These results suggest that within the young learning-disabled population there is
a group of people whose problems stem from a schizophrenic condition, but who have not been
diagnosed as such. It is therefore possible that some individuals who are diagnosed with learning
disabilities are actually suffering from schizophrenia, which has resulted in their cognitive
deficits. If diagnosed, the schizophrenic condition may respond to treatment.

Evaluation of biomedical explanations for

mental disorder
A large and impressive body of research that demonstrates a link between
biology and psychopathology has supported the biomedical model. This
in turn has led to the development of drug therapies and other biological
therapies (discussed in the next section), many of which have offered
significant help in coping with abnormal psychological functioning.
However, there are several criticisms and limitations to the approach.
First, the biomedical model is essentially a reductionist model because it
reduces the explanation of psychopathology down to its most basic
element (in this case to simple biology). The reductionist stance can
result in the neglect of some of the most important psychological causes
of behaviour and we may fail to see an individual as a whole person,
regarding them rather as a body in which some part is malfunctioning. We
may be able to explain a headache in terms of brain chemistry but that
tells us little or nothing about the possible life stresses that may have
given rise to that biological condition.
Second, although biological processes certainly do affect our behaviour,
thoughts and emotions, it is not a one-way process. We are increasingly
coming to recognise that our behaviour, thoughts and emotions affect our
biology.
Third, much of the research into the biological causes of abnormality has
been conducted on animals in which various conditions such as anxiety and
helplessness have been induced by drugs, surgery or the way they have been
conditioned. These procedures provide very little information about human
functioning. Biological explanations based on such research are often
incomplete or simply irrelevant to understanding human behaviour.
Fourth, evidence from family, twin and adoption studies indicating a link
between genetics and clinical syndromes are open to other interpreta-
tions. The closer the genetic link, the more similar the environment is

33
Angles on Atypical Psychology

likely to be. Siblings not only have certain genes in common but are quite
likely to have shared any potentially damaging experiences. We cannot
therefore conclude that genes rather than environment were responsible
for the abnormality. As mentioned earlier, there is a doubtless a complex
interaction of environment and biology and concentration on one at the
expense of the other is liable to lead us up blind alleys.
for and
against
biomedical explanations
There is a large amount of empirical research to support biological explanations of
mental disorders.

The biomedical approach tends to neglect the role pf psychological factors in the
aetiology (cause) of atypical behaviour.

Our behaviour may affect our biology, therefore even when malfunctions of the brain
or hormone imbalances occur they may be the consequence, not the cause, of
abnormal behaviour.

where to
now
?
The following are good source of further information biomedical approaches:

Murray, R., Hill, P. and McGuffin, P. (1996) The Essentials of Postgraduate Psychiatry.
Cambridge: Cambridge University Press – although a large and detailed book, this is not as
intimidating as its name suggests, and has lots of good information on biomedical approaches to
mental disorder.

Davison, G.C. and Neale, J.M. (2001) Abnormal Psychology, 8th edition. New York: Wiley
– a standard undergraduate-level text with good general information on biomedical and other
approaches to explaining mental disorder.

Therapies based on the biomedical

approach
The brain is an amazingly complex and delicate structure and has thus
been difficult to study. Because the study of the brain has been limited by
lack of technology (until modern imaging techniques such as PET and
MRI scanning were developed), the development of biological treat-
ments has lagged behind that of the psychological therapies. Often, drugs
and other biological therapies have been introduced as the result of an
accidental discovery rather than the result of systematic research into a

34
 Chapter 2 The Biomedical Model

particular condition. Nowadays, thorough research is conducted into

biological therapies, which are very commonly used. In this section we
will look at the three main biological therapies: drugs, electroconvulsive
therapy (ECT) and psychosurgery.

Drug therapies
The use of drugs to treat psychological disorders has a relatively short,
controversial history. It started in the 1950s with the discovery of
psychotropic drugs, drugs that act mainly on the brain and seem to
alleviate the symptoms of various mental disorders. These were seen by
some as a magic cure and were possibly over-prescribed without due
appreciation of their side-effects, both physical and psychological. Over
the years, research has led to a broadening of the range of available
medication. Many new drugs have been introduced that do not have the
same problems but controversy in many areas still rages.
There are four main classes of psychotropic drugs.

Anti-anxiety drugs
Anti-anxiety drugs (also known as minor tranquillisers) help people to
relax and reduce tension. An often-prescribed group of anti-anxiety drugs
are the benzodiazepines, the trade names of two of which (Valium and
Librium), have become household names. Although these drugs do
reduce anxiety, they also induce both physical and psychological
dependence, and in the 1960s this produced serious problems for those
people, mainly women, who were prescribed them for years on end.
Patients experienced such enormous problems with withdrawal
symptoms that some people have literally continued taking them for a
lifetime. Nowadays these drugs are more likely to be prescribed for very
short periods, perhaps for ‘one-off’ anxiety-provoking situations.

Antidepressants
Antidepressant drugs help elevate mood and lift depression. One of the
most recent of these drugs is fluoxetine hydrochloride, more commonly
known by its trade name of Prozac. Along with Seroxat, Prozac is one of a
group of drugs in the SSRI (selective serotonin reuptake inhibitor) class,
which was hailed as being entirely safe because people could not develop
dependence on them or overdose. However, recently concerns have been
expressed that the use of such drugs may actually increase suicide risk in
the first few weeks of treatment (Harriman 2001). There is also concern
that such drugs are being marketed for an ever-widening range of
complaints, including premenstrual tension, and are far more often
prescribed by GPs than by psychiatrists. Prozac is now so widely used and
the prescribing of it so contentious that it has been the subject of several
books and numerous newspaper articles.

35
Angles on Atypical Psychology

Antibipolar drugs
Antibipolar drugs are used to stabilise the mood of those people suffering
from bipolar disorder (discussed in Chapter 9), in which mood swings
between depression and mania. The most commonly used of these is
lithium carbonate, which is estimated to help in 70–80% of cases. The
doses, however, have to be carefully monitored or they may threaten a
person’s life (Jefferson and Geist, 1989). Despite this, lithium is often
regarded as one of the success stories of drug therapy since, as Comer
(1992) comments, ‘Administered properly ... this and related drugs
represent a true medical miracle for people who previously would have
spent their lives on an emotional roller coaster’ (p. 165).

Antipsychotic drugs
Antipsychotic drugs are used in the treatment of psychotic conditions such
as schizophrenia. The older class of drugs were the phenothiazines. A major
problem with these drugs is the side-effects of movement disorders such as
severe shaking, muscle tremors and spasms of involuntary jerky
movements. An irreversible condition known as tardive dyskinesia affects
10–20% of all patients treated over a long period of time (Sweet et al.,
1995).
As with other classes. drugs first introduced in the 1950s have been
superseded by more effective ones with fewer side-effects, for example
clozapine. This can be effective in patients who do not respond to tradi-
tional antipsychotics (Kane et al., 1998) and is actually more effective
overall (Rosenhack et al., 1999); it can, however, impair the immune
system in a very small percentage of patients. Even more recently, two
new antipsychotics have been introduced – olanzapine and risperidone –
both having fewer side-effects but being as effective as the traditional
antipsychotics (if not more so). The search for ever-more effective drugs
with fewer side-effects is ongoing.
Although they are more effective than any other single form of treatment
for schizophrenia, drugs alone are not sufficient treatment for most
sufferers. Nevertheless, combined with psychotherapy they can help
many patients with schizophrenia lead normal lives. Unfortunately, some
patients do not respond to any antipsychotic drugs.
media
watch The following extracts are taken from an article by Sarah Boseley,
published in The Guardian, 9 July 2001.
A group of psychiatrists has made a formal protest to the president of the
profession’s royal college against a drug company’s sponsorship of a
conference opening today.
They complain that the industry’s marketing distorts the mental health
agenda to the point where pills are seen as the answer to all ills.

36
 Chapter 2 The Biomedical Model

In a letter to John Cox, President of the Royal College of Psychiatrists,

the group says that money widely available for sponsoring meetings of
doctors is an attempt to persuade psychiatry to go down the biomedical
route and to ignore social circumstances that might be the true cause of
the illness.
Two consultant psychiatrists, Pat Bracken and Phillip Thomas from the
University of Bradford, members of the group that calls itself the Critical
Psychiatry Network, will join mental health service users in demon-
strating their concerns.
The group claims that ‘biomedical frameworks’ – the focus on drugs –
increasingly dominate research and education in psychiatry, in spite of
limited evidence as to how or whether the drugs work. Dr Bracken
points to a paper in the journal Ethical Human Sciences and Services last
year on the efficacy of the SSRI (selective serotonin reuptake inhibitor)
class of antidepressant, which includes Prozac, which concluded that
the drugs worked little better than dummy pills – ‘there is a less than
10% difference in the antidepressant effect of drug versus placebo’.
Dr Bracken and colleagues feel the drive to find a medical cause of all
mental illness ignores issues such as poverty, family breakdown, or other
social or cultural problems. They call for the college to pull back from
the increasingly close relationship with the pharmaceutical industry.

Questions
1 What are the implications of drug companies funding research into therapies
for certain disorders?

2 What factors are likely to be ignored if a biomedical approach is taken?

3 Why may it be tempting for state health services to concentrate on

biomedical rather than psychological therapies?

4 What ethical concerns are expressed in this article?

interactive
angles
There has been considerable media coverage of the alleged side-effects of SSRIs, and about
the allegations of dodgy practices on the part of drug companies. Carry out an Internet search,
using a search engine such as Alta Vista or Google and key words like Prozac, Seroxat, drug
companies, etc. Compile a list of arguments for and against the use of these drugs.

37
Angles on Atypical Psychology

Electroconvulsive therapy (ECT)

ECT is a procedure in which a very brief application of electricity is used
to induce a seizure. It has a fearful reputation, dating back to a time when
it was applied without anaesthetic or muscle relaxant and was almost
certainly used to subdue troublesome patients; however its modern appli-
cation is very different. The patient is anaesthetised with a fast-acting
barbiturate and given a muscle relaxant to temporarily paralyse the
muscles so they do not contract during the seizure and cause broken
bones. Electrodes are fitted to the head and a small electric current is
passed through the brain for one second or less. The resulting seizure,
monitored by an EEG machine, lasts from about 30 seconds to a minute
and the patient regains consciousness about 15 minutes later. He or she
usually experiences confusion, a headache and sometimes nausea and has
no memory for events surrounding the treatment. These symptoms
usually disappear within a few hours.
ECT is usually given 2–3 times a week for between 1 and 4 weeks, until
the patient appears recovered, then two more treatments are adminis-
tered to prevent relapse. No one knows how or why ECT works or what
the electrically stimulated seizure does to the brain. It is thought that it
acts by temporarily altering some of the brain’s electrochemical processes
(see p. 162 for a further discussion). ECT is still a very widely used form
of treatment, mainly for people whose depression is so severe that they
cannot wait 3 weeks or so for antidepressants to take effect (due to
absolute desperation and suicide risk) or for whom these drugs are
ineffective. It is also used for acute mania and certain forms of schizo-
phrenia.
The use of ECT is still highly controversial. Much of this controversy
surrounds its effectiveness, the severity and extent of the side-effects and
the lack of knowledge of how it works. There is also concern that its use
is viewed as a quick and easy solution to a problem better tackled by long-
term psychotherapy. It is very difficult to be objective about the use of
ECT because opinions about it are so extreme. Recent studies have
tended to show good effectiveness, but some side-effects. Ng et al. (2000)
administered ECT to the right hemispheres of 32 patients suffering from
major depression (see p. 156 for a discussion of major depression).
Depression scores decreased by around 50% following treatment,
although memory was found to be seriously affected when tested immedi-
ately after a 6-week course of treatment (over 30% of personal memories
were lost). However, most of this memory loss was made up within the
next month, and overall the study was supportive of the value of ECT.
Papolos (1997) claims that ECT has a higher success rate for the
treatment of severe depression than any form of treatment and that
suicide attempts are relatively rare after ECT. In a recent follow-up of 58
depressed patients, Gagne et al. (2000) found that 93% of patients who

38
 Chapter 2 The Biomedical Model

continued to have ECT and take antidepressants following an episode of

major depression remained free of symptoms 2 years later, as opposed to
52% of those who continued to take antidepressants alone. This suggests
that ECT is helpful in preventing recurrence of depression. On the other
hand, Youssef et al. (1999), in an article entitled ‘Time to Abandon
Electroconvulsion as a Treatment in Modern Psychiatry’ claims that ECT
is not superior to drugs, and that much of the improvement attributed to
ECT is an effect of placebo or possibly anaesthesia. They argue that the
treatment merely shortens the duration of an illness rather than
improving the outcome. The controversy is ongoing. However there is
now a new and exciting alternative to ECT that is painless and safe –
transcranial magnetic brain stimulation.

what’s
new
?
transcranial magnetic brain stimulation
Transcranial magnetic brain stimulation (TMS) is a non-invasive and painless method of
brain stimulation (Figure 2.4), which may offer an alternative to ECT. The method involves
the production of a magnetic field produced by a wire coil held outside the head. The
magnetic field then induces an electric current in nearby regions of the brain. Unlike
electricity, which is diffused by bone, high-intensity magnetic pulses pass readily through it, so
when a magnetic current is passed through the skull, it is possible to focus on a more specific

Figure 2.4 The TMS apparatus

39
Angles on Atypical Psychology

area of the brain than is possible with ECT. Perhaps the most crucial difference between ECT
and TMS is that the latter does not produce major motor seizures. It is therefore possible to
avoid side-effects such as transient memory loss, and an anaesthetic is unnecessary. The
treatment is usually administered daily for at least a week and is referred to as rTMS (repet-
itive TMS).
Research on rTMS gives cause for cautious optimism. George et al. (1995) conducted a pilot
study of the effect of rTMS on six long-term depressed patients who had previously not
responded to treatment. Two of them showed considerable improvement. One of the
responders, a middle-aged woman, reported feeling well for the first time in 3 years. Pridmore
et al., (2000) compared the effect of rTMS and ECT in patients suffering from major
depression who had failed to respond to at least one course of medication. Although ECT was
slightly better overall, the difference was not great. The researchers therefore concluded that
rTMS has antidepressant effects of sufficiently useful proportions to make further research
worth while. Klein (2000) similarly comments that preliminary evidence from studies of
depressed individuals suggests that it might, in some cases, offer an alternative to ECT.

Psychosurgery
Psychosurgery involves severing or otherwise disabling areas of the brain
to treat mental illness. Psychosurgery has a notorious and gory history. It
was first introduced by Moniz in 1936, at a time when there were no drugs
to treat mental illness. An operation, known as a frontal lobotomy (or
transorbital lobotomy depending on the precise technique used), was
hailed as a solution to overcrowded and understaffed asylums and mental
hospitals and performed on an estimated 50 000 people in the USA
between 1938 and the mid-1950s. These early operations were performed
with surgical knives, electrodes, suction, even ice picks, to cut or sweep
out great portions of the frontal lobe. They often left patients extremely
apathetic, intellectually impaired and with a changed personality. Many
suffered complications such as seizures and paralysis and it was not
unusual for them to die as a result of the operation. Despite this, Moniz
was awarded the Nobel Prize for Medicine in 1949.
These serious irreversible effects led to a change in procedures and the
introduction of a far more sensitive and precise operation. The intro-
duction of drugs to treat psychoses also resulted in a drastic drop in the
rate of operations. Modern psychosurgery involves the use of a computer-
based process called stereotactic magnetic resonance imaging to guide a small
electrode to the limbic system (a part of the brain concerned with emotion
and autonomic body functions). An electric current is then passed
through the electrode to burn a small lesion, about 1 cm in diameter.
A cingulotomy is the most common form of psychosurgery. It involves
cutting the cingulate gyrus, a small section of the brain that connects the
limbic system to the frontal lobes. This is performed to alleviate mental

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disorders such as major depression, bipolar disorder, chronic anxiety

states and obsessive–compulsive disorder.
Psychosurgery is very rarely used now – fewer than 25 operations are carried
out in the USA and Britain annually and only one or two in Australia. It is
a treatment of last resort after all other forms of therapy, both biological and
psychological, have been unsuccessful and is only performed with the
patient’s fully informed consent. However, there is no consensus among
practitioners as to how long other therapies should be tried before resorting
to psychosurgery. The estimated success rate is 50–67% for OCD and
55–78% for major depression and bipolar disorder, depending on the
procedure used, with few if any adverse side-effects (Cosgrove et al., 2000).
One valid criticism of psychosurgery is that there is a lack of theoretical
knowledge on which the treatment is based. In other words, when it is
successful we do not know why. Some knowledge is available, for example
that electrical stimulation of some parts of the limbic system can affect
anxiety levels and that abnormalities in glucose metabolism have been
found in specific areas of the limbic system in patients with OCD.
However, the exact nature of any dysfunction and its effect on emotion is
not yet understood.
Considerable concern continues to be expressed about any procedure
whose effects are irreversible. The organisation MIND (Darton, 2000)
draws attention to an alternative procedure tried on four patients suffering
from very severe OCD that had not responded to treatment. Electrodes
were implanted in their brains and were used to stimulate a small area of
the brain rather than destroy cells. Three of the four patients showed
improvement. In one patient the anxiety and obsessional thinking were
relieved when the stimulation was on but not when it was switched off. It
is not clear how long the treatment continued but the study did indicate
that long-term stimulation might be useful in the management of OCD.

for and
against
biomedical treatments
There is substantial evidence for the effectiveness of biomedical treatments in relieving
the symptoms of mental disorder.

Biomedical treatments sometimes have serious side-effects.

There are concerns in some quarters that drugs may be over-used because of the impor-
tance of sponsorship by drug companies.

Biomedical treatments are becoming increasingly safe and effective, and there are
innovative new treatments such as TMS.

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Angles on Atypical Psychology

where to
now
?
The following are good sources of further information on biomedical treatments:

Fancher, R.T. (1995) Cultures of Healing. New York: Freeman – takes a very critical look at
the biomedical model in general.

Glenmullen, J. (2001) Prozac Backlash. Touchstone Books – argues the case against Prozac.

Healy, D. (1993) Psychiatric Drugs Explained. Kings Lynn: Mosby – a well-written guide to
the use of psychotropic drugs.

Kramer, P. (1997) Listening to Prozac. London: Penguin – puts the case in favour of Prozac
use.

Conclusions
It is important to note that even those people who recognise that biology
may be the cause of a mental problem do not necessarily advocate
biological intervention and feel that psychological methods are appro-
priate in some cases. Indeed, rarely are biological therapies advocated as
the only means of treatment; sometimes such interventions are recom-
mended to put the patient in a frame of mind in which they are receptive
to psychological therapy. For example, in some cases of anxiety disorders
and depression, drugs may be deemed necessary to bring the individual to
a state in which they can benefit from psychological treatments. In other
conditions, such as bipolar disorder and schizophrenia, it may be necessary
for a patient to receive medication for life but these medications are likely
to be fully effective only when used alongside psychological therapies.
The use of biological therapies implies that there is a direct relationship
between biological dysfunction and mental dysfunction, but this is by no
means always the case. For example, stress causes the release of adren-
aline and noradrenaline in the bloodstream, which can then have an
adverse effect on behaviour. Rather than taking medication to reduce the
levels of these particular hormones, it is better to help the individual to
reduce their level of stress, or to help them find ways of coping with situa-
tions so that they are no longer stressful.
Biological therapies provide an invaluable and sometimes life-saving
tool in the treatment of mental disorder, and improvements in the
existing methods and better alternatives are constantly being researched.
However, it is unlikely (and probably undesirable) that biological treatments
should ever be the only help that sufferers are given. A combination of
appropriate somatic and psychological therapies is always likely to
provide the most favourable outcomes.

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 Chapter 2 The Biomedical Model

?
what
do you
know
1 Discuss ways in which the role of genetic factors in abnormal behaviour can
be investigated.

2 What role may biochemical factors play in causing abnormal behaviour?

3 Discuss arguments for and against the biomedical approach to explaining

atypical behaviour.

4 Describe and evaluate the use of two biomedical therapies for abnormal
behaviour.

5 Evaluate the use of biological therapies in treating abnormal behaviour.

43